PURPOSE:Exaggerated blood pressure (BP) response during physical exertion is associated with increased risk for cardiovascular events. Furthermore, it may be the predisposing factor for myocardial infarction triggered by physical exertion. The authors have shown that systolic BP achieved after 6 minutes of exercise is the strongest predictor of left ventricular hypertrophy. Furthermore, a 37 mm Hg increase in systolic BP above resting BP at 6 minutes of exercise was the threshold for left ventricular hypertrophy. The purpose of this study was to determine predictors of exercise BP response in normotensive and hypertensive women. METHODS:An exercise tolerance test (Bruce) was performed by 1411 normotensive (resting BP < 140/90 mm Hg) and hypertensive (resting BP > or = 140/90 mm Hg) women. These women were faculty, students, and staff at the University of Maryland, College Park, Maryland, and the George Washington University Medical Center, as well as patients undergoing a routine exercise tolerance test at West Coast Cardiology, Pinellas Park, Florida. Two fitness categories (low-fit and high-fit) were established on the basis of treadmill time to exhaustion adjusted for age. RESULTS:Significant associations were observed among the 6-minute exercise BP and age, body mass index, resting systolic and diastolic BP, heart rate, and exercise time to exhaustion. In a stepwise multiple-regression analysis, the determinants of BP after 6 minutes of exercise were resting systolic BP and treadmill time to exhaustion (R2 = 0.36) for normotensive women and treadmill time to exhaustion and resting systolic BP (R2 = 0.30) for hypertensive women. When fitness categories were contrasted, low-fit women in both the normotensive and hypertensive categories had higher BP and rate-pressure product after 6 minutes of exercise than the high-fit women (P <.05). CONCLUSIONS:Resting systolic BP and cardiorespiratory fitness are determinants of a submaximal exercise BP response for both hypertensive and normotensive women. Low cardiorespiratory fitness is associated with a higher BP response during submaximal exercise, suggesting that increased fitness may attenuate this abnormal rise in BP. Thus, low- to moderate-intensity physical activities for most days of the week should be encouraged for all women to increase cardiorespiratory fitness. This is likely to attenuate an abnormal rise in systolic BP that may occur during routine daily activities and protect against the associated health consequences.
The prevalence of systemic hypertension and its cardiovascular consequences is higher in African-Americans than in whites. Low to moderate intensity aerobic exercise lowers blood pressure (BP) in African-American patients with severe hypertension. It is not known whether such exercise can improve lipid metabolism in these patients. Thirty-six African-American men with established essential hypertension, aged 35 to 76 years, were randomly assigned to an exercise (n = 17) or no exercise (n = 19) group. The exercise group exercised for 16 weeks, 3 times/week, at 60% to 80% of maximum heart rate. After 16 weeks, peak oxygen uptake in the exercise group improved (21 ± 4 vs 23 ± 3 ml/kg/min; p <0.001). Body weight did not change. Exercise intensity correlated with high-density lipoprotein (HDL) cholesterol changes from baseline to 16 weeks (r = 0.65; p <0.01) and was the strongest predictor of these changes (R2 = 0.4; p = 0.009). Lipoprotein-lipid changes in the 2 randomized groups did not differ significantly. A 10% increase in HDL cholesterol—42 ± 19 versus 46 ± 19 mg/dl; p = 0.003—noted in 10 patients who exercised ≥75% of maximal heart rate suggested the existence of an exercise intensity threshold. Thus low to moderate intensity aerobic exercise may not be adequate to modify lipid profiles favorably in patients with severe hypertension. However, substantial changes in HDL cholesterol were noted in patients exercising at intensities ≥75% of age-predicted maximum heart rate, suggesting an exercise-intensity threshold.
BACKGROUND:Myotonic dystrophy, the most common form of adult dystrophy, has been shown to be caused by amplification of CTG triplet repeat in the 3' untranslated region of a protein kinase gene located on chromosome 19. Impaired glucose metabolism has been suggested as a possible explanation of brain and skeletal muscle involvement in this multisystem disease. We investigated whether myocardial glucose metabolism is impaired in myotonic dystrophy and whether this impairment is related to the size of the mutation.METHODS AND RESULTS:The myocardial metabolic rate for glucose (MMRGlu, mumol.min-1.g-1), K1 (blood-to-tissue transfer constant), k2 (tissue-to-blood transfer constant), and k3 (phosphorylation rate constant) were determined in 7 control subjects and 12 patients with myotonic dystrophy by using parametric images generated from dynamic cardiac positron emission tomography (PET) and 18F-fluoro-2-deoxy-glucose studies. The expansion of the CTG triplet repeats was analyzed in patients with the probe cDNA25 after EcoRI digestion. Nonparametric tests were used to compare quantitative variables between control subjects and patients. The correlations between the size of the mutation and PET parameters were studied by linear regression. MMRGlu and k3 were significantly decreased in patients compared with control subjects (0.39 +/- 0.20 versus 0.64 +/- 0.25, P = .03, and 0.09 +/- 0.07 versus 0.24 +/- 0.21, P = .03, respectively), whereas K1 and k2 were not statistically different between control subjects and patients. MMRGlu and k3 correlate inversely with the length of the CTG triplet repeat (r = -.65 and P = .03 for MMRGlu, and r = -.85 and P = .001 for k3, respectively).CONCLUSIONS:In myotonic dystrophy, the observed reductions in MMRGlu and phosphorylation are inversely linked to the length of the mutation. This observation suggests that impaired modulation of a protein kinase involved in myocardial hexokinase activation may give a pathophysiological schema to relate the molecular defect and the abnormal myocardial metabolism in myotonic dystrophy.
Electrocardiograms were recorded at baseline and regular intervals in 53 patients with myotonic dystrophy who were followed for a mean of 6.3 +/- 4.0 years. Patients with cardiac events had a significantly prolonged PR interval (p <0.001), a later age of onset of neuromuscular symptoms (p <0.05), and were older (p <0.005).
Compression of the heart outside the pericardial sac is a rare cause of hemodynamic compromise and cardiac tamponade. We report an atypical case of regional cardiac compression caused by a large loculated anaerobic bacterial empyema.
OBJECTIVE:To examine the association between miles run per week and high-density lipoprotein cholesterol levels in healthy middle-aged men.BACKGROUND:Regular exercise increases levels of high-density lipoprotein cholesterol. However, the exercise requirements for such increases are not well defined.METHODS:Healthy, nonsmoking men (n = 2906; age, 43 +/- 4 years) completed a questionnaire on health habits and physical activities and a symptom-limited exercise test. They were then stratified on the basis of the number of miles run per week. Six groups, with mileages of 0, 5, 9, 12, 17, and 31 per week, were established.RESULTS:A gradual increase in high-density lipoprotein cholesterol level was observed with increased miles (0.008-mmol/L [0.308-mg/dL] increase in high-density lipoprotein cholesterol level per mile). Most of the changes were associated with distances of 7 to 14 miles per week. Levels of low-density lipoprotein cholesterol, triglycerides, and the ratio of total cholesterol to high-density lipoprotein cholesterol also improved with weekly mileage. The high-density lipoprotein cholesterol level correlated significantly with all exercise components, anthropometric measures, and alcohol consumption. Group comparisons disclosed significant differences (P < .05) in exercise time to exhaustion, miles run per week, body fat, body weight, and body mass index. Age and alcohol consumption were similar across groups.CONCLUSIONS:These results indicate a dose-response relationship between miles run per week, high-density lipoprotein cholesterol level, and other lipoprotein-lipid levels. Most changes were noted in those who ran 7 to 14 miles per week at mild to moderate intensities. A mile-age threshold for changes in high-density lipoprotein cholesterol level was not observed. However, when compared with those of the nonexercising group, high-density lipoprotein cholesterol levels attained statistical significance at 7 or more miles per week.
Fractional area change of the left ventricle during systole, measured in the parasternal short‐axis view, is an easily calculated index of systolic function. We assessed the correlation of echocardio‐graphic left ventricular fractional area change with radionuclide ventriculography derived left ventricular ejection fraction. Forty patients who had both echocardiography and radionuclide ventriculography were studied. Nonuniformity of left ventricular function was present in 38%. For the group as a whole the correlation coefficient for fractional area change and ejection fraction was 0.82 (P < 0.001). For patients with uniform systolic function the correlation coefficient was 0.79 (P < 0.001). For those with regional differences, the correlation coefficient was 0.72 (P < 0.005). We conclude that echocardiographically derived fractional area change, measured in the parasternal short‐axis view, is an excellent measure of left ventricular function even in patients with heterogeneity of regional function.
Background. The prevalence of hypertension and its cardiovascular complications is higher in African Americans than in whites. Interventions to control blood pressure in this population are particularly important. Regular exercise lowers blood pressure in patients with mild-to-moderate hypertension, but its effects in patients with severe hypertension have not been studied. We examined the effects of moderately intense exercise on blood pressure and left ventricular hypertrophy in African-American men with severe hypertension.Methods. We randomly assigned 46 men 35 to 76 years of age to exercise plus antihypertensive medication (23 men) or antihypertensive medication alone (23 men). A total of 18 men in the exercise group completed 16 weeks of exercise, and 14 completed 32 weeks of exercise, which was performed three times per week at 60 to 80 percent of the maximal heart rate.Results. After 16 weeks, mean (+/-SD) diastolic blood pressure had decreased from 88+/-7 to 83i8 mm Hg in the patients who exercised, whereas it had increased slightly, from 88+/-6 to 90+/-7 mm Hg, in those who did not exercise (P=0.002). Diastolic blood pressure remained significantly lower after 32 weeks of exercise, even with Substantial reductions in the dose of antihypertensive medication. In addition, the thickness of the interventricular septum (P=0.03), the left ventricular mass (P=0.02), and the left-ventricular mass index (P=0.04) had decreased significantly after 16 weeks in the patients who exercised, whereas there was no significant change in the nonexercisers.Conclusions. Regular exercise reduced blood pressure and left ventricular hypertrophy in African-American men with severe hypertension.
The purpose of this study was to determine whether normalized peak rate of left ventricular area expansion during diastole, as obtained from echocardiography using the parasternal short‐axis view, correlates well with left ventricular diastolic peak filling rate, as determined from radionuclide ventriculography. Normalized peak rate of area expansion, readily calculated from tracings of the ventricular endocardium on sequential echocardiographic image frames, can be measured rapidly, noninvasively, repeatedly, and without radiation exposure. The advent of automated edge detection systems that permit continuous, on line display of ventricular areas may further enhance the utility of this technique. Twenty‐four patients with and without regional wall‐motion abnormalities who had both echocardiography and radionuclide ventriculography as part of their clinical care were analyzed. Comparing normalized peak rate of area expansion with peak filling rate, the correlation coefficient was 0.86 (P < 0.001). These findings suggest that echocardiographically derived normalized peak area expansion measured in the parasternal short‐axis view is an excellent measure of global diatstolic function.
Cardiac calcification is a common problem in patients with renal failure. Calcific deposits often affect the mitral annulus, the aortic valve, and the coronary arteries. We report an atypical case of cardiac calcification obstructing the left ventricular outflow tract with minimal aortic valve calcification.